Probable causal link between epilepsy and sleep apnea: case report.

Patients with epilepsy were reported to have concomitant sleep apnea, but it has been rarely linked to the epilepsy itself. We present a case of a 28-year-old, obese man with secondary medically resistant partial complex epilepsy due to a brain trauma, with progressive snoring, and sleep agitation, apneas, and important daytime somnolence. It was noticed in the polysomnographic study that he had several sleep respiratory events, probably due both to the epileptic seizures and the sleep apnea syndrome as a co-morbidity. Apnea and epilepsy will be discussed. A careful video-EEG-polysomnography study is important in evaluating refractory epileptic patients and/or epileptic patients with snoring.

Probable causal link between epilepsy and sleep apnea: case report

Patients with epilepsy were reported to have concomitant sleep apnea, but it has been rarely linked to the epilepsy itself. We present a case of a 28-year-old, obese man with secondary medically resistant partial complex epilepsy due to a brain trauma, with progressive snoring, and sleep agitation, apneas, and important daytime somnolence. It was noticed in the polysomnographic study that he had several sleep respiratory events, probably due both to the epileptic seizures and the sleep apnea syndrome as a co-morbidity. Apnea and epilepsy will be discussed. A careful video-EEG-polysomnography study is important in evaluating refractory epileptic patients and/or epileptic patients with snoring.

Pacientes com epilepsia e concomitante apnéia do sono já foram descritos na literatura, mas raramente foram associados à epilepsia como fator causal desta apnéia. Nós apresentamos o caso de um homem com 28 anos, obeso, com epilepsia parcial complexa farmacorresistente secundária a trauma crânio encefálico e roncos progressivos, sono agitado, apnéias, além de importante sonolência diurna. Foram observados, durante estudo polissonográfico, freqüentes eventos respiratórios durante o sono, provavelmente secundários a crise epilética, além da síndrome de apnéia obstrutiva do sono como uma co-morbidade. Um exame cuidadoso de vídeo-EEG-polissonografia do caso é importante na avaliação de pacientes com epilepsia fármaco resistente e/ou epilépticos com roncos.

[Transient lesion in the splenium of the corpus callosum in epileptic child with cerebral low grade glioma]. / Lesão transitória no esplênio do corpo caloso em criança epiléptica com glioma cerebral de baixo grau.

We report on a seven years-old boy with complex partial seizures and the presence of low grade glioma in left fronto-parietal region. The magnetic resonance imaging showed focal non-hemorrhagic lesion in the splenium of the corpus callosum. The description of the transient lesion in the splenium of the corpus callosum was related in three previous studies, in patients with epilepsy. Thus, the observed transient focal lesion in the splenium of the corpus callosum of this child, probably, has correlation with to prolonged focal partial seizures and not to the presence of glioma low grade.

Lesão transitória no esplênio do corpo caloso em criança epiléptica com glioma cerebral de baixo grau / Transient lesion in the splenium of the corpus callosum in epileptic child with cerebral low grade glioma

Trata-se do relato de caso de menino de sete anos com crises epilépticas parciais complexas secundárias à presença de glioma de baixo grau em região fronto-temporal esquerda, cuja ressonância magnética evidenciou, lesão transitória focal do esplênio do corpo caloso. A revisão bibliográfica através de pesquisa no database MedLine resultou no encontro de descrição de lesão transitória do esplênio do corpo caloso foi relatada em três estudos anteriores, em pacientes portadores de epilepsia. Portanto, a lesão transitória observada no corpo caloso desta criança, provavelmente, tem correlação com as crises epilépticas do lobo temporal e não à presença do glioma de baixo grau cerebral.

Secondary hypogammaglobilinemia after use of carbamazepine: case report and review.

Immunologic disorders related to anticonvulsant therapy have been described in the last three decades, including cellular and humoral alterations that result in recurrent infections; however, the physiopathologic mechanisms are not completely understood. This report describes a patient with complex partial epilepsy and hypogammaglobulinemia while in treatment with carbamazepine, with significant improvement in clinical signs and laboratory tests after substitution to sodium valproate. The authors stress the importance of clinical and laboratory evaluation of patients in continuous anticonvulsant therapy, including immunoglobulins levels and peripheral blood evaluations.

Complex partial seizures and aphasia as initial manifestations of non-ketotic hyperglycemia. Case report.

We describe a case of non-ketotic hyperglycemia (NKH), heralded by complex partial seizures and aphasia of epileptic origin, besides versive and partial motor seizures. This clinical picture was accompanied by left fronto-temporal spikes in the EEG. The seizures were controlled by carbamazepine only after the control of the diabetes. A month later, carbamazepine was discontinued. The patient remained without seizures, with normal language, using only glybenclamide. Complex partial seizures, opposed to simple partial seizures, are rarely described in association to NKH. Epileptic activity localized over language regions can manifest as aphasia.

Complex partial seizures and aphasia as initial manifestations of non-ketotic hyperglycemia: case report

We describe a case of non-ketotic hyperglycemia (NKH), heralded by complex partial seizures and aphasia of epileptic origin, besides versive and partial motor seizures. This clinical picture was accompanied by left fronto-temporal spikes in the EEG. The seizures were controlled by carbamazepine only after the control of the diabetes. A month later, carbamazepine was discontinued. The patient remained without seizures, with normal language, using only glybenclamide. Complex partial seizures, opposed to simple partial seizures, are rarely described in association to NKH. Epileptic activity localized over language regions can manifest as aphasia.

High doses of carbamazepine for refractory partial epilepsy

Forty-eight patients with partial seizures were analysed during treatment with 1200 mg/d or more of carabamazepine (CBZ). Thirty-three were on monotherapy and fifteen on polytherapy. The other drugs, were kept unchanged in the patients on polytherapy. The dose of CBZ was increased if no control was observed and the patient had no side effects. The doses used ranged between 1200 and 1900 mg/day 91200 mg/day, n=18; 1300 mg/day, n=l: 1400 mg/day, n=7: 1600 mg/day, n=9; 1700 mg/day, n=4; 1800 mg/day, n=8; 1900 mg/day, n=1). Anticonvulsant plasma levels were taken to confirm patient compliance. The average plasma level was 9.6 ug/mL. The period of follow up varied from 3 to 96 months (M=25,6). Seizure's control was observed in 7 (14.48 per cent) patients taking 1200 mg/day and in 2 (4.16 per cent patients taking 1400 mg/day of CBZ. Thirty-nine patients did not show any control (81.21 per cent). Ten patients (20.81 per cent) had signs of intoxication. When patients have no improvement with 1400 mg/day, it is difficult to obtain any control despite the use of higher doses of CBZ, which frequently expose the patient to signiflcant side effects.

Effects of conventional antiepileptic drugs in a model of spontaneous recurrent seizures in rats.

Pilocarpine (PILO) induces in rats limbic seizures that become secondarily generalized and evolve to status epilepticus (SE). Spontaneous recurrent seizures are registered during the long-term period following the systemic administration of PILO in rats. EEG, behavioral, and pathological features resemble those of complex partial seizures. The antiepileptic drugs (AEDs) diazepam, phenobarbital (PB), valproic acid (VPA) and trimethadione protect against PILO-induced SE while phenytoin (PHT) and carbamazepine (CBZ) are ineffective. Studies with AEDs on spontaneous seizures (chronic period) of this model have not yet been established. We now report the effects of different AEDs on spontaneous seizures. Male Wistar rats were subjected to PILO-induced SE. Following recovery from SE animals were daily observed in order to detect spontaneous seizures and to establish the baseline seizure frequency. PB 40 mg/kg, PHT 100 mg/kg, CBZ 120 mg/kg, VPA (450 mg/kg and 600 mg/kg) and ethosuximide (ETX) 400 mg/kg were given daily to epileptic rats for two weeks during the spontaneous recurrent seizures period. PB, CBZ and PHT were effective against spontaneous seizures. VPA was also effective against spontaneous seizures at the dose of 600 mg/kg and ETX was inactive against these seizures. Such pharmacological profiles correlate well with complex partial seizures. The results indicate that spontaneous recurrent seizures after PILO-induced SE may be a useful model for finding new AEDs with better efficacy against complex partial seizures. The use of animal models that share both pharmacological and phenomenological features with human epilepsy might improve their predictive value for specific types of human epilepsy.